• BMB Reports
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• v.42 no.1
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• pp.28-34
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• 2009

To understand the molecular mechanism underlying proline accumulation in Brassica napus, cDNAs encoding ${\Delta}^1$-pyrroline-5-carboxylate synthetase (BnP5CS), ornithine $\delta$-aminotransferase (BnOAT) and proline dehydrogenase (BnPDH) were isolated and characterized. Southern blot analysis of BnP5CSs in B. napus and its diploid ancestors suggested a gene loss may have occurred during evolution. The expression of BnP5CS1 and BnP5CS2 was induced, while the expression of BnPDH was inhibited under salt stress, ABA treatment and dehydration, prior to proline accumulation. The upregulation of BnOAT expression was only detected during prolonged severe osmotic stress. Our results indicate that stress-induced proline accumulation in B. napus results from the reciprocal action of activated biosynthesis and inhibited proline degradation. Whether the ornithine pathway is activated depends on the severity of stress. During development, proline content was high in reproductive organs and was accompanied by markedly high expression of BnP5CS and BnPDH, suggesting possible roles of proline during flower development.

• Biomedical Science Letters
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• v.16 no.4
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• pp.359-363
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• 2010

The miniature pig is a very suitable donor species in xenotransplantation of human organs. Intestine ischemia/reperfusion (I/R) is associated with high morbidity and mortality. Endoplasmic reticulum (ER) stress and apoptosis has been associated with the onset of diverse diseases. Thus, we examined the effect of intestine I/R on the expression of ER stress and apotptosis related molecules. In the present study, I/R induced phosphorylation of protein kinase-like endoplasmic reticulum kinase (PERK), IRE, and ATF-4. I/R also increased the expression of the proapoptotic transcription factor CAAT/enhancer-binding protein homologous protein (CHOP). In addition, I/R decreased the expression of Bcl-2, but increased the expression of Bax, cleaved PARP, and cleaved caspase-3. Moreover, I/R increased splicing form of XBP-1 mRNA and the expression of caspase-6 and caspase-3 mRNA. In conclusion, intestine I/R induced ER stress and apoptosis in miniature pig.

• Annals of Clinical Neurophysiology
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• v.25 no.1
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• pp.32-37
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• 2023

Background: Type 2 diabetic mellitus (T2DM) is an emerging global pandemic which is associated with lots of co-morbidities and reported vascular dysfunctions. T2DM associated vascular dysfunctions leads to vasculopathy in the form of altered peripheral vascular dynamics. Cold stress test (CST) is a reliable sympathetic reactivity test used for assessing vascular dysfunctions. In this study we are trying to quantify vascular dysfunctions in T2DM patients non invasively by various parameters of photoplethysmography (PPG) of cold stress test. Methods: Case control study had done in referral health center AIIMS, Raipur. Parameters are recorded by finger-PPG before, during and after CST (1 min) in 2 groups, control (n = 20 healthy volunteers) and case (n = 20 diagnosed T2DM patients). Results: Due to cold stress, PPG parameter peak amplitude was significantly decreased in both healthy and T2DM groups (p <0.001 and p <0.001, respectively). However, recovery trend of amplitude was significantly slow in T2DM compared to healthy subjects. Another PPG parameter peak to peak interval was significantly higher in healthy group compared to T2DM patients. Conclusions: This study showed that T2DM patients has significant deranged pulse volume parameters like amplitude and peak to peak interval can be used to objectively quantify the vasculopathy in T2DM patients by using sympathetic reactivity to cold stress.

• Journal of Yeungnam Medical Science
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• v.38 no.2
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• pp.83-94
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• 2021

The global obesity epidemic and the growing elderly population largely contribute to the increasing incidence of type 2 diabetes. Insulin resistance acts as a critical link between the present obesity pandemic and type 2 diabetes. Naturally occurring reactive oxygen species (ROS) regulate intracellular signaling and are kept in balance by the antioxidant system. However, the imbalance between ROS production and antioxidant capacity causes ROS accumulation and induces oxidative stress. Oxidative stress interrupts insulin-mediated intracellular signaling pathways, as supported by studies involving genetic modification of antioxidant enzymes in experimental rodents. In addition, a close association between oxidative stress and insulin resistance has been reported in numerous human studies. However, the controversial results with the use of antioxidants in type 2 diabetes raise the question of whether oxidative stress plays a critical role in insulin resistance. In this review article, we discuss the relevance of oxidative stress to insulin resistance based on genetically modified animal models and human trials.

• Molecules and Cells
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• v.41 no.1
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• pp.3-10
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• 2018

Autophagy is one of the major degradative mechanisms that can eliminate excessive nutrients, toxic protein aggregates, damaged organelles and invading microorganisms. In response to obesity and obesity-associated lipotoxic, proteotoxic and oxidative stresses, autophagy plays an essential role in maintaining physiological homeostasis. However, obesity and its associated stress insults can often interfere with the autophagic process through various mechanisms, which result in further aggravation of obesity-related metabolic pathologies in multiple metabolic organs. Paradoxically, inhibition of autophagy, within specific contexts, indirectly produces beneficial effects that can alleviate several detrimental consequences of obesity. In this minireview, we will provide a brief discussion about our current understanding of the impact of obesity on autophagy and the role of autophagy dysregulation in modulating obesity-associated pathological outcomes.

• Proceedings of the Korean Biophysical Society Conference
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• 2002.06b
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• pp.34-34
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• 2002

Oxidative stress has been considered as a major cause of inducing cell damage, but it is recently recognized that mild oxidative stress or receptor-mediated production of ROS contributes to the regulation of various cellular functions. Several ion channels, such as L-type $Ca^{2＋}$ channels and $Ca^{2＋}$-activated $K^{＋}$ channels, have been shown to be regulated by oxidation of thiol group in their structure, and are suggested to be involved in ROS-sensitive cellular signaling.(omitted)

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.7
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• pp.1031-1034
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• 1999

Circulating lymphocytes collected from control and heat-stressed buffaloes were subjected to in vitro culture with glucocorticoids, epinephrine or serotonin and their effect, if any, on the release of intracellular prolactin (PRL) was studied using ELISA and C-ELISA techniques. It was noted from the study that PRL level was higher in lymphocytes than in plasma of the control and heat-stressed animals, and that the PRL levels increased in the plasma of heat-stressed animals compared to that of non stressed animals with a significant decrease in lymphocytic PRL content by heat stress. Epinephrine and serotonin significantly increased the release of intracellular PRL from the lymphocytes of both in the control and the heat-stressed buffaloes but release of PRL from lymphocyte was not significantly changed by cortisol treatment in both control and heat-stressed buffaloes as compared to epinephrine and serotonin in vitro. When lympocytes were incubated with serotonin, it caused drastic lysis of the lymphocytes but epinephirine and cortisol did not show any lysis. It may be concluded from this study that hormones like epinephrine or serotonin known to increase during stress, release intracellular PRL from lymphocytes, the satellite PRL storage/synthesizing organ of blood, although the mechanism of the release is different.

• Asian-Australasian Journal of Animal Sciences
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• v.23 no.11
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• pp.1462-1468
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• 2010

The effects of vitamin C and vitamin E with selenium on acid-base balance and some stress hormones were evaluated during heat stress in goats. Goats, 1.5 years of age, were divided into control, heat stress and antioxidant treatment groups 1, 2 and 3. Except for the control, all groups were exposed to a temperature of $40{\pm}2^{\circ}C$ with a relative humidity of 30% for 5 h/d for 21 days in a psychrometric chamber. Rectal temperature and respiratory rates were recorded daily post exposure. Blood samples were collected on every 3rd day for estimation of plasma vitamins C and E, total antioxidant activity and hormones, and separate blood samples were taken to estimate acid-base status. The rectal temperature and respiratory rates were increased (p<0.05) in the heat stress group only. Except for pH and $pO_2$, which were increased significantly (p<0.05) other parameters of acid-base balance such as $pCO_2$, $HCO_3^-$, $TCO_2$, BEb, BEcef, PCV and Hb were significantly decreased (p<0.05) in the heat stress group. An improvement in acid-base status was noted in the antioxidant supplemented groups. Prolactin and cortisol levels were significantly (p<0.05) higher and free T3 and T4 levels were significantly (p<0.05) lower in the heat stress group. Levels of prolactin and cortisol were decreased and free T3 and T4 were increased in antioxidant treatment groups. Different levels of antioxidant supplementation resulted in similar protection against heat stress.

• Journal of Ginseng Research
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• v.34 no.2
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• pp.132-137
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• 2010

Lead (Pb) is a metal that is generally considered to be toxic to the cardiovascular system. Pb-exposed animals display the evidence of increased oxidative stress and hypertension. The current study was designed to examine whether Korean red ginseng (KRG) has protective effects against Pb-induced hypertension and oxidative stress in Pb-exposed rats. Male Sprague-Dawley rats were randomly assigned to Pb exposure or control groups. KRG was administered in drinking water at a concentration of 100 mg/kg/day; the control group received plain drinking water. Animals in the Pb-exposed groups were provided with drinking water containing 100 ppm Pb acetate for 12 weeks. Blood pressure, plasma glutathione, blood Pb concentration, and hematologic data, such as red blood cell quantity, were determined. Pb poisoning was assessed by measuring the blood Pb concentration. Pb exposure (100 ppm) for 12 weeks resulted in a marked rise in systolic blood pressure and blood Pb concentration, as well as a significant reduction in plasma glutathione levels and red blood cell quantity. Other measurements, such as heart rate, body weight, and white blood cell quantity, were unchanged. Treatment with KRG significantly lowered blood pressure, raised plasma glutathione and increased red blood cell numbers in Pb-exposed animals; it also had no effect on heart rate, body weight, or white blood cell quantity. However, the elevated blood Pb concentration was not reduced by treatment with KRG (100 mg/kg). Taken together, these data indicate that treatment with KRG in Pb-exposed animals can reduce oxidative stress and lower blood pressure, suggesting that KRG might be protective against Pb-exposed hypertension and oxidative stress.

• Archives of Pharmacal Research
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• v.28 no.12
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• pp.1358-1364
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• 2005

In this study, we investigated whether a novel anti-ischemic $K_{ATP}$ opener KR-31378 [(2S,3S,4R)­N'-cyano-N-(6-amino-3,4-dihydro-3-hydroxy-2 -methly-2-dimethoxymethly-2H-benzopyran-4-yl)­N'-benzylguanidine] has protective effect against oxidative stress-induced death in heart-derived H9c2 cells. Cell death was induced by BSO, butionine sulfoximine, which inhibits GSH synthesis and subsequently increases reactive oxygen species (ROS) level. Cell death was quantitatively determined by measuring lactate dehydrogenase (LDH) activity and stained by Hoechst 33258. BSO-induced ROS production and mitochondrial membrane potential (MMP) were measured using 2',7'-dichlorofluorescein diacetate oxidation and rhodamine 123, respectively. Both the LDH release and the ROS elevation induced by treatment of H9c2 cells with 10 mM BSO, were significantly decreased by KR-31378. These protective effect and antioxidant effect of KR-31378 appeared to be independent on $K_{ATP}$ channel opening. Cells exposed to BSO showed an early reduction in MMP, and this reduction in MMP was significantly reversed by treatment with KR-31378. Caspase-3 activity in BSO treated H9c2 cells was remarkably increased, and this increased caspase-3 activity was significantly reversed by KR-31378. In conclusion, our results suggest that KR-31378 can produce cardioprotective effect against oxidative stress-induced cell death through antioxidant mechanism.